Reddy SSK, Chaiban JT. The Endocrinology of Aging: A Key To Longevity "Great Expectations". Endocr Pract 2017;23:1107-16. http://journals.aace.com/doi/10.4158/EP171793.RA
To find the fountain of youth, to defeat the ravages of time and prevent aging and to strive for the utmost longevity have been romantic goals of humanity for eons. Scientific endeavors in this arena have been ambitious in this area but overcome by the reality of the complexity of such a simple idea. Aging suggests a process that may affect every system variably. Some may develop type 2 diabetes, while others may manifest osteoarthritis or dementia. The causes for these various disorders may be different.
At a superficial level, many may equate anti-aging with longevity but in reality, living longer denotes duration of life and not the quality of life. Thus, healthy aging is not necessarily equal to increased longevity. Longevity itself is a moving target: a few millennia ago, surviving childhood to reproductive age was a major accomplishment. Today, reaching a century of life is within reach for many. In this review, we will not address aspects of treating endocrine disease in the elderly but rather discuss endocrine pathophysiology and management of the aging process itself.
We cannot deny that modern medicine and technological advances- through easier access to health care, nutrition and sanitation, the advent of vaccination and the development of newer medications- have had a great effect on longevity and health span. For example, the average lifespan in Belgium, France and England in the 19th century was 32 - 33 years compared with 47.5, 78.8 and 87.2 years in Sierra Leone, United States and Monaco respectively in our contemporary age. Not all people age at the same rate and longevity differs between regions, families and individuals. Throughout the centuries, human society has tried to identify predictors of longevity and decipher the secrets for extended healthy longevity.
As can be anticipated, there will be neither a single etiology for the process of aging nor a single therapeutic reversal agent. One of the hallmarks of aging across species is telomere erosion. Shalev and Belsky support a “two-hit” hypothesis: Adverse events in infancy or childhood compounded by a second hit of sexual maturation and reproductive stress. Clinical observations of perinatal and childhood adversity resulting in late-life disease and increased fertility, reduced longevity in birds and mammals, as well as in primates. As expected, the data is mixed in human studies.
If one believes that the prime directive for any organism is to perpetuate its genetic material, then the same processes favoring earlier reproduction will also lead to premature aging. At the cellular level, mitochondrial function, oxidative stress and inflammatory processes affect this telomere pathology. Childhood adversity may be mediating its effects via epigenetic changes.
Arising out of these concepts are models of aging. Quality of life emphasis is the major difference in schools of thought favoring anti-aging or successful aging. i.e. longevity alone is an insufficient goal. In the last two decades, the consideration of social determinants of health has enhanced the traditional medical model.
Since endocrine function is critical for growth and development as well as for reproductive health, hormonal regulation of the aging process has been of great interest. For an excellent overview of metabolic basis of longevity, refer to the review by Lopez-Otin et al. Resultant menopause, andropause, somatopause, and also adrenopause have major impact on the older population’s well-being and autonomy leading to loss of muscle mass and strength, osteopenia and osteoporosis with secondary falls, increased cardiovascular disease and other metabolic changes and propensity to obesity. Herein, we will discuss the lessons learned from comparative biology as well as from studies of the insulin-IGF-1 axis, the thyroid and reproductive axes. In addition, we will briefly review other biological determinants with close association with hormonal function.
To find the fountain of youth, to defeat the ravages of time and prevent aging and to strive for the utmost longevity have been romantic goals of humanity for eons. Scientific endeavors in this arena have been ambitious in this area but overcome by the reality of the complexity of such a simple idea. Aging suggests a process that may affect every system variably. Some may develop type 2 diabetes, while others may manifest osteoarthritis or dementia. The causes for these various disorders may be different.
At a superficial level, many may equate anti-aging with longevity but in reality, living longer denotes duration of life and not the quality of life. Thus, healthy aging is not necessarily equal to increased longevity. Longevity itself is a moving target: a few millennia ago, surviving childhood to reproductive age was a major accomplishment. Today, reaching a century of life is within reach for many. In this review, we will not address aspects of treating endocrine disease in the elderly but rather discuss endocrine pathophysiology and management of the aging process itself.
We cannot deny that modern medicine and technological advances- through easier access to health care, nutrition and sanitation, the advent of vaccination and the development of newer medications- have had a great effect on longevity and health span. For example, the average lifespan in Belgium, France and England in the 19th century was 32 - 33 years compared with 47.5, 78.8 and 87.2 years in Sierra Leone, United States and Monaco respectively in our contemporary age. Not all people age at the same rate and longevity differs between regions, families and individuals. Throughout the centuries, human society has tried to identify predictors of longevity and decipher the secrets for extended healthy longevity.
As can be anticipated, there will be neither a single etiology for the process of aging nor a single therapeutic reversal agent. One of the hallmarks of aging across species is telomere erosion. Shalev and Belsky support a “two-hit” hypothesis: Adverse events in infancy or childhood compounded by a second hit of sexual maturation and reproductive stress. Clinical observations of perinatal and childhood adversity resulting in late-life disease and increased fertility, reduced longevity in birds and mammals, as well as in primates. As expected, the data is mixed in human studies.
If one believes that the prime directive for any organism is to perpetuate its genetic material, then the same processes favoring earlier reproduction will also lead to premature aging. At the cellular level, mitochondrial function, oxidative stress and inflammatory processes affect this telomere pathology. Childhood adversity may be mediating its effects via epigenetic changes.
Arising out of these concepts are models of aging. Quality of life emphasis is the major difference in schools of thought favoring anti-aging or successful aging. i.e. longevity alone is an insufficient goal. In the last two decades, the consideration of social determinants of health has enhanced the traditional medical model.
Since endocrine function is critical for growth and development as well as for reproductive health, hormonal regulation of the aging process has been of great interest. For an excellent overview of metabolic basis of longevity, refer to the review by Lopez-Otin et al. Resultant menopause, andropause, somatopause, and also adrenopause have major impact on the older population’s well-being and autonomy leading to loss of muscle mass and strength, osteopenia and osteoporosis with secondary falls, increased cardiovascular disease and other metabolic changes and propensity to obesity. Herein, we will discuss the lessons learned from comparative biology as well as from studies of the insulin-IGF-1 axis, the thyroid and reproductive axes. In addition, we will briefly review other biological determinants with close association with hormonal function.
